Analysis of the 3′ Terminal Sequence Recognized by the Rift Valley Fever Virus Transcription Complex in Its Ambisense S Segment

Préhaud, Christophe; López, Nora; Blok, Marinus J.; Obry, Véronique; Bouloy, Michèle

doi:10.1006/viro.1996.8324

Cited by 47 publications

(34 citation statements)

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“…Thus, it will greatly improve the chances of developing urgently needed prophylactic measures and more feasible therapeutic interventions. The established helper virus system can already be used to modify the viral genome segments and study the impact on the viral replication cycle, as demonstrated before for other bunyaviruses (1,6,10,13,25,33,40). Insertions of genetic markers into the viral genome will later facilitate the identification of recombinant viruses and document reassortment events.…”

Section: Discussionmentioning

confidence: 99%

Reverse Genetics for Crimean-Congo Hemorrhagic Fever Virus

Flick

Feldmann

et al. 2003

J Virol

102

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The widespread geographical distribution of Crimean-Congo hemorrhagic fever (CCHF) virus (more than 30 countries) and its ability to produce severe human disease with high mortality rates (up to 60%) make CCHF a major public health concern worldwide. We describe here the successful establishment of a reverse genetics technology for CCHF virus, a member of the genus Nairovirus, family Bunyaviridae. The RNA polymerase I (pol I) system was used to generate artificial viral RNA genome segments (minigenomes), which contained different reporter genes in antisense (virus RNA) or sense (virus-complementary RNA) orientation flanked by the noncoding regions of the CCHF virus S segment. Reporter gene expression was observed in different eukaryotic cell lines following transfection and subsequent superinfection with CCHF virus, confirming encapsidation, transcription, and replication of the pol I-derived minigenomes. The successful transfer of reporter gene activity to fresh cells demonstrated the generation of recombinant CCHF viruses, thereby confirming the packaging of the pol I-derived minigenomes into progeny viruses. The system offers a unique opportunity to study the biology of nairoviruses and to develop therapeutic and prophylactic measures against CCHF infections. In addition, we demonstrated for the first time that the human pol I system can be used to develop reverse genetics approaches for viruses in the family Bunyaviridae. This is important since it might facilitate the manipulation of bunyaviruses with cell and host tropisms restricted to primates.

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Section: Discussionmentioning

confidence: 99%

Reverse Genetics for Crimean-Congo Hemorrhagic Fever Virus

Flick

Feldmann

et al. 2003

J Virol

102

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“…Thus, deletion of the first 3Ј-terminal three nucleotides of the genome promoter of respiratory syncytial virus had no effect on promoter activity (7), whereas influenza A virus genome promoter lacking the first 3Ј nucleotides retained about 60% of wild-type promoter activity (21). Moreover, the 3Ј-terminal first two nucleotides of the S RNA of the phlebovirus Rift Valley Fever virus were not required for the transcriptional activity of the S genome promoter (34).…”

Section: Vol 79 2005mentioning

confidence: 95%

Functional Characterization of the Genomic Promoter of Borna Disease Virus (BDV): Implications of 3′-Terminal Sequence Heterogeneity for BDV Persistence

Rosario

Perez

Torre

2005

J Virol

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Borna disease virus (BDV) is an enveloped virus with a genome organization characteristic of Mononegavirales. However, based on its unique features, BDV is considered the prototypic member of a new virus family, Bornaviridae, within the order Mononegavirales. We have described the establishment of a reverse genetics system for the rescue of BDV RNA analogues, or minigenomes, that is based on the use of polymerase I/polymerase II. Using this BDV minigenome rescue system, we have examined the functional implications of the reported sequence heterogeneity found at the 5 and 3 termini of the BDV genome and also defined the minimal BDV genomic promoter within the 3-terminal 25 nucleotides. Our results suggest that the accumulation of RNA genome species containing truncations of one to three nucleotides at their 3 termini may contribute to modulate BDV RNA replication and gene expression during long-term persistence.Borna disease virus (BDV) causes central nervous system disease in a variety of vertebrate species, which is frequently manifested by behavioral abnormalities (20,33,37). However, both viral and host factors can influence symptoms and pathology associated with BDV infection (18-20, 35, 37, 43). Serologic and molecular epidemiological data indicate that the natural host range of BDV as well as its prevalence and geographic distribution are very broad (19,20,(35)(36)(37)43). Moreover, there is evidence that BDV can infect humans, being possibly associated with certain neuropsychiatric disorders (2,5,31,(35)(36)(37)43).BDV is an enveloped virus with a nonsegmented, negativestrand RNA genome. Its genome (ca. 8.9 kb), the smallest among known nonsegmented, negative-strand RNA viruses, has an organization similar to that of other mononegaviruses (12,40). Six major open reading frames are found in the BDV genome sequence (3Ј-N-p10/P-M-G-L-5Ј) (12,40). BDV has the property, unique among known animal nonsegmented, negative-strand RNA viruses, of a nuclear site for the replication and transcription of its genome (3, 9). Moreover, BDV uses a remarkable diversity of strategies, including RNA splicing, for the regulation of its genome expression (10,12,40,41,45). Based on its distinct features among known mononegaviruses, BDV is considered the prototypic member of a new virus family, Bornaviridae, within the order Mononegavirales.We have established an RNA polymerase I/polymerase II system for intracellular reconstitution of BDV RNA replication and transcription (30). In this system, a BDV RNA analog, or minigenome, is intracellularly synthesized by the cellular RNA polymerase I. This BDV minigenome RNA contains the BDV 5Ј and 3Ј untranslated regions cis-acting sequences required for RNA synthesis mediated by the BDV polymerase (30,39,40,42). Encapsidation of the polymerase I-derived BDV minigenome RNA by plasmid-supplied BDV N and P generates a template that is recognized by the intracellularly reconstituted BDV polymerase to direct synthesis of fulllength antiminigenome RNA (replicate) and a subgenomic mRNA (transcri...

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“…Among the family Bunyaviridae, the establishment of a reverse genetics system has been reported only for BUNV (5), while minigenome (or minireplicon) systems have been developed in BUNV (13), LACV (3), Crimean-Congo hemorrhagic fever virus (15), Hantaan virus (14), UUKV (16), and RVFV (1,21,26). In a typical minigenome system, virus-like RNA (minigenome) transcripts contain an internal open reading frame (ORF) of a reporter gene in place of a viral ORF sandwiched by untranslated regions (UTR) of viral RNA termini.…”

mentioning

confidence: 99%